Pancreas Flashcards
what are the SENDAI criteria?
Sendai Criteria (2012) for BD-IPMN = “SEDNAIL”
High risk features = progress to surgery
- Scleral icterus – obstructive jaundice
- Enhancing solid component
- Duct – MPD >10mm
Worrisome features = progress to EUS + FNA
- Nodularity – mural nodules
- Abrupt change or atrophy – abrupt change in PD or distal pancreatic atrophy
- Inches – size of cyst >3cm
- Lipase – clinical pancreatitis
What is SIRS?
Definition;
- clinical syndrome that is a form of dysregulated inflammation following an insult.
- It occurs when inflammatory mediators produced in response to an insult spill over into the systemic circulation.
Parameters;
- Body temperature less than 36 °C or greater than 38 °C
- Heart rate greater than 90 beats per minute
- Tachypnea greater than 20 breaths per minute; or, an arterial partial pressure of carbon dioxide less than 4.3 kPa (32 mmHg)
- WCC count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms). Band forms greater than 3% is called bandemia or a “left-shift.”
What is the pathophysiology of SIRS?
Pro-inflammatory mediators (TNF, IL-1, IL-6) spillover into systemic circulation and activate
- Complement cascade
- C3a + C5a vasodilatation + endothelial damage (leaky capillaries)
- Coagulation cascade
- extrinsic pathway = hypercoaguable
- Lipids
- PG, TXA2, PAF
Characterized by VPAM
- Vasodilatation (nitric oxide)
- Permeability of capillaries (interleukins)
- Activation of complement and coagulation cascade (extrinsic pathway)
-
Metabolic response
- fever
- RAAS activation = fluid + salt retention
- Glucocorticoid/Catecholamine release = hyperglycaemia, catabolic state
What is the pathophysiology of pancreatitis?
“ACINARS”
- Activation – proteolytic enzmes activated in acini
- Co-localisation - zymogen granules (trypsinogen) and lysozymes (cathepsin). Both together = trypsin
- Injury– trypsin damages acinar cell and activates more trypsinogen which causes more cell injury
- Neutralize – natural defenses against injury are to remove damaged cells (apoptosis via capases) and/or remove trypsinogen through trypsinogen inhibitors (SPINK-1, chymotrypsin)
- Autodigestion – ongoing pancreatic injury and release of enzymes
- Release – inflammatory cytokines (IL-1, IL6, TNF)
- Systemic - SIRS
Why is enteral feeding better than TPN in pancreatitis?
Enteral feeding reduces SIMS SIRS, Infections, Mortality, Surgery need) as preserves GUT mucosal integrity and prevents bacterial translocation into portal circulation and evidence states unequivocally better than TPN
Timing of ERCP in pancreatitis?
- cholangitis
- biliary obstruction – suspected biochemically (worsening LFTs) or radiologically (visible stone, dilated duct)
How can you tell the difference between a mucinous cystadenoma and IPMN?
Imaging
- Ducts involved and dilated in IPMN whereas not for MCN.
FNA
- both will have mucin and high CEA however only IPMN will have high amylase levels.
Managment of symptomatic pancreatic pseudocyst persisting after expectant managment
MRCP = ductal connection or not?
2 key questions
Does it connect with pancreatic duct?
- if yes = transpapillary stenting (ERCP)
Where is it located?
- stomach = cyst-enterostomy
- spleen = distal pancreatectomy, cyst-enterostomy
What are the histological types of IPMN?
GIPO
Gastric, Intestinal, Pancreaticobiliary and Oncocytic
Role of pre-operative biliary drainage in resectable obstructive jaundice?
- Controversial and conflicting results in literature but preoperative ERCP
- may be associated with increased infectious and fistula complications.
- No impact on mortality or LOS after surgery.
- Useful if want to allow time for neoadjuvant treatment or patient is symptomatic (cholangitis, pruritis)
How do you define resectable, borderline resectable and locally advanced pancreatic cancer?
As per American HPBA (simplified)
Resectable (STAGE I/II)
- No abutment or encasement of major vessels
Borderline Resectable
- SMV/PV = abutment/encasement but reconstructable
- SMA/CHA = <180° or 50% abutment of tumour
- Coeliac Axis = No abutment or encasement
Locally Advanced (STAGE III)
- SMV/PV = involved but not reconstructable
- SMA/CHA = encasement
When do you biopsy pancreatic cancer?
- metastatic disease or locally advanced disease
- wanting to exclude autoimmune pancreatitis
- if neoadjuvant treatment is being contemplated (eg, for a borderline resectable lesion)
- if alternative diagnoses need to be excluded (eg, metastatic disease to the pancreas).
What are the indications for diagnostic laparoscopy in pancreatic cancer?
ROUTINE
- one-third of patients thought to be resectable by state of the art imaging will be found to be unresectable based upon laparoscopic findings
SELECTIVE
- size of primary > 3 cm
- CA 19-9 > 100
- undergoing neoadjuvant chemotherapy
What type of stent do you use if a patient presents with obstructive jaundice due to pancreatic cancer?
Types of stents
- plastic
- metal
Plastic
- PROS = cheaper, easily replaceable
- CONS = increased stent occlusion (repeated ERCP), stent patency is only about 3 months
Metal
- PROS = longer stent patency (8-12 months), less risk of obstruction,
- CONS = expensive, difficult to replace, Malignant disease must be established before inserting
What are the risk factors for pancreatic cancer?
- syndromes - Peutz Jeugher, BRCA-2, Lynch Syndrome
- Smoking
